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Fasting as a Therapy in Neurological Disease


Fasting as a Therapy in Neurological Disease

Matthew C L Phillips. Nutrients.


Fasting is deeply entrenched in evolution, yet its potential applications to today's most common, disabling neurological diseases remain relatively unexplored. Fasting induces an altered metabolic state that optimizes neuron bioenergetics, plasticity, and resilience in a way that may counteract a broad array of neurological disorders. In both animals and humans, fasting prevents and treats the metabolic syndrome, a major risk factor for many neurological diseases. In animals, fasting probably prevents the formation of tumors, possibly treats established tumors, and improves tumor responses to chemotherapy. In human cancers, including cancers that involve the brain, fasting ameliorates chemotherapy-related adverse effects and may protect normal cells from chemotherapy. Fasting improves cognition, stalls age-related cognitive decline, usually slows neurodegeneration, reduces brain damage and enhances functional recovery after stroke, and mitigates the pathological and clinical features of epilepsy and multiple sclerosis in animal models. Primarily due to a lack of research, the evidence supporting fasting as a treatment in human neurological disorders, including neurodegeneration, stroke, epilepsy, and multiple sclerosis, is indirect or non-existent. Given the strength of the animal evidence, many exciting discoveries may lie ahead, awaiting future investigations into the viability of fasting as a therapy in neurological disease.

Keywords: cancer; epilepsy; fasting; metabolic syndrome; multiple sclerosis; neurodegeneration; neurological disease; stroke; therapy.

Conflict of interest statement

The author declares no conflict of interest.


Figure 1
Figure 1
Fasting-induced metabolic and transcriptional mechanisms and their effects on neurons (BHB—beta-hydroxybutyrate; BDNF—brain-derived neurotrophic factor; PGC1α—peroxisome proliferator-activated receptor γ coactivator 1α; AMPK—AMP-activated protein kinase; mTOR—mammalian target of rapamycin; IL6—interleukin 6; TNFα—tumor necrosis factor α).

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